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Anticoagulants and anti-anemia > anticoagulants and anti-anemic power point > Flashcards

anticoagulants and anti-anemic power point Flashcards

1
Q

confers biologic activity upon prothrombin and factors VII, IX, and X by participating their postribosomal modifications

A

vitamin K

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2
Q

is an essential cofactor in the carboxylation of several glutamate residues in prothrombin and factors VII, IX, and X

A

vitamin K

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3
Q

onset of effect is delayed for 6 hours but the effect is complete by 24 hours then treating depression of prothrombin activity by excess warfarin or vitamin K deficiency

A

vitamin K

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4
Q

vitamin k has poor bioavailability following ______ administration

A

SQ

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5
Q

increases the factor VIII activity

A

desmopressin acetate

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6
Q

classic hemophilia, or hemophilia A

A

factor VIII deficiency

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7
Q

christmas disease, or hemophilia B

A

factor IX deficiency

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8
Q

concentrate contains activated clotting factors

A

factor IX

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9
Q

is a plasma protein fraction obtainable from whole blood containing fibrinogen

A

cryoprecipitate

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10
Q

Anticoagulation and fibrinolysis:

A

1.Degrades the clot by tissue-type or urokinase-type plasminogen activator
Endothelial cells secrete t-PA (fibrinolysis) at sites of injury, rapidly inactivated in blood
2.Thrombomodulin -blocks coagulation cascade by binding thrombin leading to inactivation of factor V and VIII
3.Release of prostacyclin-inhibits platelet aggregation and vasoconstriction
4. Antithrombin III- surface heparin-like molecules and blocks coagulation cascade
5.Tissue factor pathway inhibitor- inhibits extrinsic coagulation pathway

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11
Q

binds thrombin leading to inactivation of factors V and VIII…this blocks coagulation cascade

A

thrombomodulin

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12
Q

inhibits platelet degranulation, aggregation and vasoconstriction

A

prostacyclin

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13
Q

serine protease inhibitor, binds to and inactivates factors IIa, IXa, Xa, Xla, and Xlla

A

Antithrombin III

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14
Q

inhibits extrinsic coagulation pathway

A

tissue factor pathway inhibitor

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15
Q

surface heparin-like molecules (blocks coagulation cascade)

A

Antithrombin III

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16
Q

3 types of pharmacological interventions to treat thrombosis

A
  1. antiplatelet
  2. anticoagulant
  3. thrombolytic
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17
Q

The 4 major steps for hemostasis

A
  1. local vasoconstriction
  2. formation of primary hemostatic plug
  3. formation of thrombus (fibrin containing blood clot)
  4. fibrinolysis- degradation of blood clot
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18
Q

3 steps in primary hemostais: the platelet plug

A
  1. Vasucular injury- exposes reactive subendothelial matirix proteins
  2. Platelet adhesion and activation- TXA2 and integrin (IIb/IIIa)
  3. Platelet granule release- ADP activates integrin receptor, TXA2, calcium release
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19
Q

What happens during platelet adhesion and activation?

A
  • Thromboxane A2 (TXA2) released- is a potent vasoconstrictor and platelet activator
  • Conformational change in the integrin (IIb)/IIIa) receptor, restulting in fibringogen binding
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20
Q

What 3 molecules are released during platelet granule release?

A
  1. ADP- activates integrin receptor (IIb/IIIa)
  2. TXA2
  3. Calcium
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21
Q

activates integrin receptor (IIb/IIIa)

A

ADP

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22
Q

The secondary hemostasis: coagulation process involves:

A

Is a clotting cascade that leads to thrombin activation ad formation of fibrin fibers to stabilize hemostatic plug
Thrombin is the final active protease
The cascade is initiated via the Intrinsic and extrinsic system.
vitamin k is required to be activated throughout the intrinsic system, extrinsic system, and final common pathway.
In the final common pathway vitamin k is required to be activated for the production of prothrombin—> thrombin—>fibrinogen—->fibrin

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23
Q

important for clotting factors

A

calcium

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24
Q

The central role of thrombin in coaulation :
1.
2.
3.

A
  1. activates multiple clotting factors
  2. potent platelet activator
  3. activates factor XIII to cross-links the fibrin polymer (cross-linked fibrin polymer is responsible for fibrin degradation products)
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25
Q

prevent primary hemostastic plug formation

A

antiplatelet drugs

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26
Q

inhibit clotting cascade to ultimately prevent fibrin clot formation

A

anticoagulant drugs

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27
Q

dissolve an existing clot by digesting fibrin

A

thrombolytic drugs

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28
Q 
Antiplatelet drugs:
1.
2.
3.
4.
5.
6.
A
  1. ASA
  2. Dipyridamole
  3. Clopidogrel
  4. Ticlopidine
  5. Abciximab
  6. Eptifibatide
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29
Q

selectively inhibits the synthesis of thromboxe A2 (which causes platelet aggregation and granule) by irreversible acetylation of the exzyme cyclooxygenase (COX-1)

A

ASA

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30
Q

Rapid absorption-peak (plasma) 15-20 minpost administration

A

ASA

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31
Q

Higher dose leads to inhibition of prostacyclin production and reduced efficacy of therapy

A

ASA

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32
Q

This effect persist for platelet lifespan 7-10 days

A

ASA

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33
Q

Adverse effects: increased incidence of hemorrhagic stroke; GI bleeding, tinnitus, Reye’s syndrome for young people

A

ASA

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34
Q

vasodilator that inhibits platelet function by inhibition of phosphodieserase (PDE), leads to increased intracellular cAMP levels which reduces intracellular calcium and inhibits platelet activation

A

Dipyridamole

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35
Q

Inhibits thromboxane synthase, therefore lowering the levels of TXA2 production

A

Dipyridamole

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36
Q

Short duraction of action. Primary therapeutic use is in combination with ASA to prevent cerebrovascular ischemia

A

Dipyridamole

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37
Q

Blocks P2Y12 receptor. Is a prodrug metabolized by CYP2C19, duration of the antiplatelet effect is 7-10 days

A

Clopidogrel

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38
Q

Therapuetic uses:
Reduction of the rate of stroke, MI, heart attack, unstable angina and death in patients with recent MI or stroke, peripheral arterial disease, or acute coronary syndrome. Is equivalent to ASA in the prevention of stroke

A

Clopidogrel

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39
Q

Adverse effects:
Prolonged bleeding, thrombotic thrombocytopenic purpura, FDA black box warning about CYP2C19 poor metabolizers are at high risk of treatment failure and a greater risk for major adverse CV events.

A

Clopidogrel

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40
Q

Irreversibly inhibits the P2y 12 ADP receptor.

A

Ticlopidine

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41
Q

ADP receptor blockade inhibits activation of the glycoprotein IIb/IIIa pathway. Activation of the IIb/IIIa receptor complex is the final common pathway for platelet aggregation and is important in the cross linking of platelets by fibrin

A

Ticlopidine

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42
Q

Therapuetic uses:
used as standard practice in combination with ASA (synergistically) to prevent stent thrombosis. Typically used for patients who are intolerant/allergic to ASA

A

Ticlopidine

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43
Q

Adverse effects:
Most common nausea/vomiting, diarrhea, hemorrhage.
Severe neutropenia
Rare: thrombotic thrombocytopenic purpura (TTP) (1 in 1600-4800)

A

Ticlopidine

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44
Q

Integrin receptor GPIIb/IIIa inhibitors:
1.
2.

A

Abciximab

Eptifibatide

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45
Q

Fab fragment of humanized monoclonal antibody directed against the GFPIIb receptor

A

Abciximab

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46
Q

Therapeutic uses:
when used with ASA and heparin to treat coronary thromboses or during coronary angioplasty, reduces restenosis, recurrent MI

A

Abciximab

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47
Q

Adverse effects: major hemorrhagic event 1%-10% patients, long duration of action-approx 10hours

A

Abciximab

48
Q

Cyclic peptide inhibitor of the fibrinogen binding on the GPIIb receptor

A

Eptifibatide

49
Q

Therapeutic uses:

acute coronary synrome and for angioplastic coronary interventions

A

Eptifibatide

50
Q

Adverse effects:

major hemorrhage in 10% of patients

A

Eptifibatide

51
Q

act on clotting factors present in plasma to either inhibit pro-clotting factors or activate anti-clotting factors

A

anticoagulants

52
Q

prevent synthesis of factors via vitamin K

A

anticoagulants

53
Q

like antiplatelet drugs, cannot dissolve a thrombus that has already formed

A

anticoagulants

54
Q

catalyzed inhibition of cloting factors IXa, Xa and thrombin by greatly enhancing antitrombin III activity (approximatey 1000 fold) by causing conformational hange in ATIII exposing its reactive site

A

HMW Heparin

anticoagulant

55
Q
  • Testing required to determine dose effect on coagulation.
  • Not absorbed by GI tract due to large molecular weight therefore use IV or SQ injection, IM injection can cause hemotomas
A

HMW Heparin

anticoagulant

56
Q

short half life (approx 1h) means frequent injections or continuouis infusion-not suitable in outpatient setting

A

HMW Heparin

anticoagulant

57
Q

therapeutic use:

venous thrombosis and pulmaonary embolism, angina, acute MI

A

HMW Heparin

anticoagulant

58
Q

Does not cross the placenta: therefore is the drug of choice for anticoagulation during pregnancy

A

HMW Heparin

anticoagulant

59
Q

contraindications:
hemorrhage (particularly intracrania) hemophilia, thrombocytopenia, hypertension, surgery of the brain, spinal cord or eye

A

HMW Heparin

anticoagulant

60
Q

adverse effects:

hemorrhage, osteoporosis and spontaneous fractures, 1-4 % patients get HIT (systemic hypercoabulable state

A

HMW Heparin

anticoagulant

61
Q

antagonist for HMW heparin. it combines with heparin forming a stable complex devoid of anticoaulant activity

A

protamine sulfate

62
Q

fractionated forms of HMW heparin

A

Dalteparin

low molecular weight heparins

63
Q

inhibit factor Xa by antithrombin, because the majority of molecules are of insufficient length to catalyze inhibition of thrombin

A

low molecular weight heparins

64
Q

therapeutic use:

treat venous thromboembolism, thrombosis, pulmonary embolism, and unstable angina

A

low molecular weight heparins

65
Q

neutralization of LMW heparin by protamine is

A

incomplete

66
Q

advantages over unfractionated heparin:
longer half life (4 hours) and faster absorption time, much lower risk of thrombocytopenia and oseoporosis, once daily SQ injection administered in out pt setting, less frequent monitoring required due to more predictabl pharmacokinetic response

A

low molecular weight heparins

67
Q 
Name 4 direct thrombin inhibitors:
1.
2.
3.
4.
A
  1. hirudin
  2. argatroban
  3. bivalirudin
  4. dabigatran etexilate
68
Q

bind to the active site of thrombin, therby inhibiting thrombin’s downstream effects

A

direct thrombin inhibitors

anticoagulant

69
Q

specific, irreversible thrombin inhibitor used in patients with or at risk of heparin-induced thrombocytopenia

A

hirudin
(direct thrombin inhibitor)
(anticoagulant)

70
Q

reversible thrombin inhibitor used in patients with or at risk of heparin-induced thrombocytopenia

A

argatroban
(direct thrombin inhibitor)
(anticoagulant)

71
Q
  • directly occupies the catalytic site of thrombin

* used in percutaneous coronary angioplasty

A

bivalirudin
(direct thrombin inhibitor)
(anticoagulant)

72
Q
  • Standard oral twice daily dose
  • Low molecular weight pro-drug, rapidly (approx 1h) converted to active form, which binds to exosite 1 on thrombin preventing fibrinogen cleavage to insoluble fibrin
A

dabigatran etexilate
(direct thrombin inhibitor)
(anticoagulant)

73
Q

therapeutic uses:

stroke prevention in patients with atrial fibrillation-equal efficacy to warfarin, less patient monitoring

A

dabigatran etexilate
(direct thrombin inhibitor)
(anticoagulant)

74
Q

adverse effects:

hemorrhage, hearburn, stomach upset, increase in risk of MI

A

dabigatran etexilate
(direct thrombin inhibitor)
(anticoagulant)

75
Q

benefits:

no patient monitoring/titration as with warfarin, rapid onset of action, no adverse drug reactions

A

dabigatran etexilate
(direct thrombin inhibitor)
(anticoagulant)

76
Q

dicoumarol first isolated from sweet clover silage-caused hemorrhagic disease in cattle

A

warfarin

anticoagulant

77
Q
  • blocks the carboxylation of glutamate residues in prothrombin and factors VII,IX, and X
  • results in biologically inactive coagulation factor molecules
A

warfarin

anticoagulant

78
Q

the enzyme that catalyzes the carboxylation reaction, vitamin K epoxide reductase, is inhibited by therapeutic doses, preventing reductive metabolism of the inactive vitamin K epoxide to its active hydoquinone form

A

warfarin

anticoagulant

79
Q

slow onset of action (8-12 hours)—existing clotting factors must be depleted; maximal effect 3-5 days after administration

A

warfarin

anticoagulant

80
Q

therapeutic use:
acute DVT, pulmonary embolism, venous thromboembolism, folling acute MI, prosthetic heart valve placement, chronic atrial fib

A

warfarin

anticoagulant

81
Q

adverse effects:

  • hemorrhage, risk increases with intensity and duration of therapy
  • readily crosses the placenta, can cause hemorrhage at any time and developmental defects during the 1st trimester
A

warfarin

anticoagulant

82
Q

drug interactions:
increase effects:
ASA, anabolic sterioids, antibiotics, tamoxifen, oral hypoglycemics, vitamin K deficiency

A

warfarin

anticoagulant

83
Q

drug interactions:
decrease effects:
* chronic alcohol abuse, oral contraceptives, corticosteroids, barbituates, increased hpatic synthesis of clotting factors, increased vitamin K intake, cholestryramine binds to this in the intestine and resuces its absorption and bioavailability
* metabolized by CYP2C9

A

warfarin

anticoagulant

84
Q

used to reverse warfarin associated bleeding

A

phytonadione (vitamin K 1)

85
Q

effective only if used rapidly after onset of thrombosis

A

thrombolytics

86
Q

therapeutic uses-in hospital:

acute ischemic stroke, MI, pulmonary embolism, severe deep venous thrombosis, ascending thrombophlebitis

A

thrombolytics

87
Q
  • inhibitor of thrombolytics

* inhibits the conversion of plasminogen to plasmin

A

aminocaproic acid

88
Q

most dangerous side effect is hemorrhage, of which intracranial hemorrhage is the most serious

A

thrombolytics

89
Q

contraindications: brain tumor, aneurysm, hemorrhagic stroke, major surgery within the last 2 weeks, active bleeding in GI or urinary tract, severe platelet shortage or coagulation disorder, severe uncontrolled HTN

A

thrombolytics

90
Q

hematopoiesis requires a constant supply of tree essential nutrients___________,_________,______- as well as the presence of hematopoietic growth factors

A

iron
vitamin B12
Folic acid

91
Q

Normal values of hemoglobin in females and males:

A

females: 14 (+/-) 2
males: 16 (+/-) 2

92
Q

normal values of hematocrit in females and males:

A

females: 42(+/-) 5
males: 47 (+/-) 5

93
Q

normal values of reticulocytes in females and males:

A

1 for both

94
Q

normal value for mean corpuscular hemoglobin

A

32-36

95
Q

in the absence of adequate iron, small pale erythrocytes with insufficient hemoglobin are formed (microcytic hypochromic RBC)

A

iron deficiency anemia

96
Q

3 oral iron medications for iron deiciency anemia:

A

ferrous sulfate
ferrous gluconate
ferrous fumarate

97
Q

treatment with oral iron should be continued for

A

3-6 months to replienish iron stores

98
Q

may inhibit absorption of ferrous compounds

A

antacids

99
Q

increases the absorption of iron by approx 30%

A

ascorbic acid

100
Q

adverse effects:

nausea, heartburn, epigastric discomfort, abdominal cramps, constipation, and diarrhea

A

oral iron therapy

101
Q
  • large amounts are toxic

* necrotizing gastroenteritis, vomiting, abdominal pain, bloody diarrhea, shock, letheragy, and cardiovasuclar collapse

A

iron toxicity

102
Q

treatment of iron toxicity:
1.
2.

A
  1. whole bowel irrigation to flush out unabsorbed pills
  2. deferoxamin (iron chelating compound) given systemically binds absorbed oron and promotes its excretion in urine and feces
103
Q

iron-deficient patients for which oral ron is not sufficient and pregnant women to create iron stores

A

parental iron therapy

104
Q

adverse effects:

  • acute hypersensitivity, including anaphylatic shock
  • headache, malaise, fever, nausea and vomiting, back pain, clushing, bronchospasm, nausea and vomiting
A

parental iron therapy

105
Q
  • is a cofactor for RBC maturation
  • lack of this causes abnormal DNA replication and ineffective hematopoiesis leading to megaloblastic anemia
  • absorbed from gut in an intrinsic factor
A

vitamin b 12 deficiency

106
Q
  • treatment of vitamin b 12 deficiency

* limited value if patient has deficiency of intrinsic factor

A

oral vitamin b12 supplement

107
Q
  • this vitamin b 12 therapy must be maintained for life

* IM every 4 weeks is sufficient to maintain a normal concentration of vitamin b 12

A

cyanocobalamin

108
Q
  • used for IM treatment for vitamin b 12 deficiency
  • now becoming more common as is more highly protein-bound and therfore remains longer in the circulation reducing regularity of injections
A

hydroxocobalamin

109
Q

required for essential biochemical reactions that mediate synthesis of amino acids, purines, dna, and the maturation of RBCs

A

folic acid

110
Q
  • deficency results in megaloblastic anemia microscopically indistinguishable from vitamin b12 deficiency anemia
A

folate

111
Q

causes:

  • inadequate levels in diet or impaired absorpton (intestinal disease or small bowel resection)
  • often seen in alcoholics with por diet, during pregnancy and lactation, patients with hemolytic anemia, cancer or renal dialysis
A

folic acid deficiency

112
Q

drug side effects:

  • methotrxate, trimethoprim and pyrimethamin, inhibit dihyrofolate reductase and may result in a deficiency
  • oral contrceptives and anticonvulsants impair aborption and storage
A

folic acid deficiency

113
Q

treatment of folic acid deficiency:
1.
2.

A
  1. folic acid oral tablets/MVI comboinations
  2. folinic acid (leucovorin calcium)- 5 formyl derivative of tetrahydrofolic acid-more expensive than folic acid and no greather benefit
114
Q

for anemia treatment:

maintain hgb levels between

A

11-13

115
Q

for iron therapy keep ferritin

A

> 100

116
Q

for anemia treatment: use ____________stimulating agents or transfusions

A

erythropoietin

Anticoagulants and anti-anemia (1 decks)

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